atrial fibrillation after pericardial reconstruction using extracellular matrix (NCT01247974) have not yet

been reported.

Reconstruction of the pericardium is important when there is a risk of cardiac herniation. When resection of

the pericardium is required during pneumonectomy due to a central lung tumor or an extrapleural

pneumonectomy for mesothelioma, the pericardium should be reconstructed to prevent herniation into

the empty hemithorax.32 Cardiac herniation must be quickly recognized if the patient becomes

hypotensive postoperatively. The pericardial defect is reconstructed with a 0.1-mm Gore-Tex mesh. The

mesh should be fenestrated with small incisions to allow fluid to escape decreasing the risk of

tamponade. Reconstruction of the pericardium may also help to prevent inflammatory epicarditis which

can lead to constrictive physiology after extrapleural pneumonectomy.33

PERICARDIECTOMY

Pericardiectomy is most commonly performed for constrictive pericarditis. It can be performed through

a median sternotomy or a left anterior thoracotomy in the fifth intercostal space. Anterior thoracotomy

allows removal of the pericardium over the left ventricle with minimal manipulation. Femoral

cannulation is used if bypass is necessary. Median sternotomy is the most common approach (Fig. 86-9).

Cardiopulmonary bypass increases the risk of bleeding and is used when significant cardiac

manipulation is needed or the dissection is difficult. The pericardium over the left ventricle is resected

first to avoid pulmonary edema from the right ventricle ejecting against a constricted left ventricle. The

pericardium is removed from phrenic nerve to phrenic nerve. Some patients have an immediate

improvement in hemodynamics and symptoms while others do not improve until weeks or months later.

A delayed or incomplete response is thought to be due to an incomplete resection of the visceral

pericardium or myocardial atrophy and fibrosis. Left ventricular function returned to normal in 40% of

patients.

Perioperative mortality has been reported between 5% and 15% and is due to low cardiac output,

sepsis, bleeding, and renal or respiratory failure.34 Seventy percent of mortality is due to low cardiac

output. Mortality is directly related to the patient’s preoperative status

35 and is 1% for New York Heart

Association class I to II, 10% for class III, and 46% for class IV.36 Five-year survival is 84%, and 99% of

late survivors were class I or II. Patients with constriction due to radiotherapy have a higher mortality

which may be due to radiation-induced myocardial injury. Other poor prognostic factors are renal

failure, advanced age, pulmonary hypertension, hyponatremia, and reduced cardiac output.34,37

Figure 86-9. Pericardiectomy is most commonly approached through a median sternotomy. A: The pericardium is incised, and the

fibrous pericardium dissected from the left ventricle. B: The heart is retracted to the right so that the pericardium can be resected

from phrenic nerve to phrenic nerve.

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2. Beck C, Griswald RA. Pericardiectomy in the treatment of the Pick syndrome: experimental and

clinical observations. Arch Surg 1930;21:1064.

3. Kussmaul A. Ueber schwielige Mediatino-perikarditis und dem Paradoxen Puls. Berl Klin Wochenschr

1873;10:433.

4. Karanaeff P. Paracentese des Brustkastens und des Pericardiums. Med Z 1840;9:251.

5. Rehn L. Zurexperimentellen pathologic des herzbeutels. Verh Dtsch Ges Chir 1913;42:339.

6. Sadler T. Langman’s Medical Embryology. 7th ed. Baltimore, MD: Williams & Wilkins; 1995.

7. Gibson AT, Segal MB. A study of the composition of pericardial fluid with special reference to the

probable mechanism of fluid formation. J Physiol 1978;277:367–377.

8. Spodick DH. Macrophysiology, microphysiology, and anatomy of the pericardium: a synopsis. Am

Heart J 1992;124:1046–1051.

9. Moncada R, Kotler MN, Churchill RJ, et al. Multimodality approach to pericardial imaging.

Cardiovasc Clin 1986;17:409–441.

10. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet 2004;363:717–727.

11. Brady WJ, Perron AD, Martin ML, et al. Cause of ST segment abnormality in ED chest pain

patients. Am J Emerg Med 2001;19:25–28.

12. Imazio M, Demichelis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol

2003;42:2144–2148.

13. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004;351:2195–2202.

14. Heidenreich PA, Eisenberg MJ, Kee LL, et al. Pericardial effusion in AIDS. Incidence and survival.

Circulation 1995;92:3229–3234.

15. Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608–3616.

16. Strang JI, Kakaza HH, Gibson DG, et al. Controlled clinical trial of complete open surgical drainage

and of prednisolone in treatment of tuberculous pericardial effusion in Transkei. Lancet 1988;2:759–

764.

17. Sagrista-Sauleda J, Barrabes JA, Permanyer-Miralda G, et al. Purulent pericarditis: review of a 20-

year experience in a general hospital. J Am Coll Cardiol 1993;22:1661–1665.

18. Dressler W. A post-myocardial infarction syndrome; preliminary report of a complication

resembling idiopathic, recurrent, benign pericarditis. J Am Med Assoc 1956;160:1379–1383.

19. Little WC, Freeman GL. Pericardial disease. Circulation 2006;113:1622–1632.

20. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of

pericardial diseases executive summary; the Task force on the diagnosis and management of

pericardial diseases of the European society of cardiology. Eur Heart J 2004;25:587–610.

21. Ben-Horin S, Bank I, Guetta V, et al. Large symptomatic pericardial effusion as the presentation of

unrecognized cancer: a study in 173 consecutive patients undergoing pericardiocentesis. Medicine

(Baltimore) 2006;85:49–53.

22. Ditchey R, Engler R, LeWinter M, et al. The role of the right heart in acute cardiac tamponade in

dogs. Circ Res 1981;48:701–710.

23. Beck C. Two cardiac compression triads. JAMA 1935;104:714.

24. Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive

pericarditis. Am J Cardiol 1970;26:480–489.

25. Talreja DR, Edwards WD, Danielson GK, et al. Constrictive pericarditis in 26 patients with

histologically normal pericardial thickness. Circulation 2003;108:1852–1857.

26. Abdalla IA, Murray RD, Lee JC, et al. Does rapid volume loading during transesophageal

echocardiography differentiate constrictive pericarditis from restrictive cardiomyopathy?

Echocardiography 2002;19:125–134.

27. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive

cardiomyopathy by Doppler echocardiography. Circulation 1989;79:357–370.

28. Ben-Horin S, Shinfeld A, Kachel E, et al. The composition of normal pericardial fluid and its

implications for diagnosing pericardial effusions. Am J Med 2005;118:636–640.

29. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic

echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes

spanning 21 years. Mayo Clin Proc 2002;77:429–436.

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30. Dantas CE, Sa MP, Bastos ES, et al. Pericardium closure after heart operations: a safety option? Rev

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31. Boyd WD, Johnson WE 3rd, Sultan PK, et al. Pericardial reconstruction using an extracellular

matrix implant correlates with reduced risk of postoperative atrial fibrillation in coronary artery

bypass surgery patients. Heart Surg Forum 2010;13:E311–E316.

32. Kobayashi H, Nomori H, Mori T, et al. Extrapleural pneumonectomy with reconstruction of

diaphragm and pericardium using autologous materials. Ann Thorac Surg 2009;87:1630–1632.

33. Byrne JG, Karavas AN, Colson YL, et al. Cardiac decortication (epicardiectomy) for occult

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34. Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical

spectrum and impact on outcome after pericardiectomy. Circulation 1999;100:1380–1386.

35. Seifert FC, Miller DC, Oesterle SN, et al. Surgical treatment of constrictive pericarditis: analysis of

outcome and diagnostic error. Circulation 1985;72:II264–II273.

36. McCaughan BC, Schaff HV, Piehler JM, et al. Early and late results of pericardiectomy for

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37. Bertog SC, Thambidorai SK, Parakh K, et al. Constrictive pericarditis: etiology and cause-specific

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Chapter 87

Vascular Diagnostics: The Noninvasive Vascular

Laboratory

Gregory L. Moneta

Key Points

1 Duplex ultrasound consists of a combination of gray-scale imaging and pulse Doppler. Because the

speed of sound is relatively constant in tissue, with a pulse Doppler it can be determined when an

echo is generated and when it is received. This provides range resolution enabling the operator of

the duplex machine to precisely sample and interrogate blood flow at a known location.

2 When a sound wave encounters moving reflectors, such as red blood cells, the frequency of the

reflected wave changes from that of the original wave generated by the transducer. This relationship

is reflected in the Doppler equation: fr − fo = [(2fov)/c] cos θ, Where fr is the received frequency, fo

is the originating frequency, v is the velocity of the reflector, c is the speed of sound in tissue, and θ

is the angle of the incident sound beam with the moving reflectors, the so-called Doppler angle.

3 Arterial Doppler waveforms reflect the resistance of the circulation supplied by the artery being

examined. Low resistance circulations such as cerebral and renal circulations have relatively high

amounts of diastolic flow whereas high-resistance circulations, such as extremity arteries have little

flow at the end of diastole.

4 Carotid stenosis is determined primarily from measurement of peak systolic velocity (PSV) and enddiastolic velocity (EDV) from pulse Doppler waveforms using criteria agreed upon in a national

consensus conference.

5 Air plethysmography can be used to display pulse volume waveforms. Pulse volume recordings

(PVRs) are obtained with partially inflated blood pressure cuffs that detect volume changes

sequentially down a limb. Volume changes beneath the cuffs resulting from the pulse wave result in

small pressure changes within the cuffs. These changes are displayed as arterial waveforms with the

use of appropriate transducers and provide an overall measure of the arterial circulation in an

extremity.

6 The ankle brachial index (ABI) is determined by dividing the higher ipsilateral dorsal pedal or

posterior tibial artery pressure by the higher of the two brachial artery systolic pressures and is

highly sensitive and specific for documenting the presence or absence of lower extremity arterial

occlusive disease.

7 Measurement of ankle pressures after exercise can be used to confirm arterial disease as an etiology

for exercise-associated leg pain. Failure of the ankle pressure to drop with exercise along with failure

of the ABI to decrease 20% with exercise, combined with a normal resting ABI, substantially rules

out arterial insufficiency as an etiology of exercise-induced complaints of leg pain.

8 Duplex ultrasound can detect hemodynamically significant stenosis in abdominal arteries: a PSV in

the superior mesenteric artery (SMA) of 275 cm/s or more indicates a ≥70% SMA stenosis, a celiac

artery PSV of ≥200 cm/s indicates a ≥70% celiac artery stenosis whereas a ratio of the PSV in a

renal artery to that in the aorta (renal–aortic ratio, RAR) of ≥3.5 indicates a ≥60% diameterreducing renal artery stenosis.

9 The primary ultrasound diagnostic criterion for diagnosis of venous thrombosis is failure of the vein

to collapse with application of pressure with the ultrasound probe.

10 In the upright position, venous reflux stimulated by cuff deflation that lasts >0.5 to 1 second is

indicative of pathologic venous reflux.

The noninvasive vascular laboratory provides accurate, safe, and objective evidence of the presence and

physiologic significance of vascular disease throughout the body. Two broad categories of testing are

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available in the noninvasive vascular laboratory; those based on plethysmographic techniques, and those

based on ultrasound-based techniques.

PLETHYSMOGRAPHY

Plethysmographic techniques detect volume changes in limbs that occur in response to arterial and

venous disease. The technology can be modified to determine digital pressures and produce pulse

waveforms. Examples of plethysmographic techniques include mercury strain gauge plethysmography,

air plethysmography (pulse volume recordings [PVRs]), and photoplethysmography.

ULTRASOUND

Ultrasound techniques, in particular duplex ultrasound-based technique, have largely eclipsed

plethysmographic techniques. Duplex ultrasound, introduced in 1974, was first applied to carotid

arteries. The technique combines information from ultrasound-generated images (B-mode) and Doppler

analysis of blood flow direction and velocity, hence the term “duplex.” Duplex ultrasound is currently

extensively employed for evaluation of carotid arteries, intra-abdominal arteries and veins and upper

and lower extremity arteries and veins. Since inception duplex ultrasound has advanced through: (1)

improved B-mode imaging, (2) better low-frequency scan heads permitting deeper penetration of the

ultrasound beam from the skin surface, (3) improvements in online computer-based microprocessor

software, and (4) perhaps, most importantly, the addition of color flow to the B-mode image.

Color flow superimposes a real-time color image of blood flow onto a standard gray-scale B-mode

picture. Returning echoes from stationary tissues generate the B-mode image, whereas those interacting

with moving substances (blood) generate a significant enough phase shift that they can be processed

separately and color-coded by operator selection to give information on direction and velocity of blood

flow according to the magnitude and direction of the Doppler frequency shift. It is color flow, combined

with the ability of the current generation of duplex scanners to detect very low blood flow velocities

(<5 cm/s), which makes duplex scanning practical on a routine basis throughout the body. Color flow

permits more rapid identification of vessels to be examined and is essential for duplex examination of

some vessels such as tibial arteries and veins.

BASICS OF DUPLEX ULTRASOUND

An ultrasonic wave is produced in tissue by placing a vibrating source in contact with the tissue. In

medical ultrasound the vibrating source is the ultrasound transducer contained within the ultrasound

scan head. The scan head steers and focuses the sound beam arising from the transducer, functions

crucial in deriving an ultrasound image from returning echoes.

Ultrasound transducers convert electrical energy into vibrational energy and, conversely, turn

vibrational energy of returning echoes into electrical signals that can be analyzed by the software of the

duplex machine. The design of the transducer determines the frequency of the vibrations which in turn

determines the wavelength of the sound wave produced. The relationship between frequency and

wavelength is expressed mathematically as follows:

Where λ is the wavelength, c is the speed of sound in tissue and f is the incident frequency.

The speed of sound in soft tissues averages 1,540 m/s and varies only minimally from this average in

soft tissues insonated in clinical applications of duplex ultrasound. The wavelength of the sound beam is

the primary determinant of how well the ultrasound beam penetrates the tissue. Because the speed of

sound within the tissue is, for all practical purposes, constant (1,540 m/s), the ability of ultrasound to

penetrate tissue depends on the frequency of the vibrating source (transducer). As noted above,

transducer frequency is determined by the design of the transducer and is thus controlled by the

manufacturer of the duplex device. For examination of the carotid artery, transducer frequencies of 5 to

7.5 MHz provide optimal tissue penetration for clinical purposes.

As noted above the term duplex refers to the combination of Doppler and B-mode (“B” stands for

“brightness”) ultrasound in the same device. Both types of ultrasound require analysis of reflected

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